Lung Endothelial Cell Apoptosis During Ischemic Acute Kidney Injury

Shock ◽  
2012 ◽  
Vol 38 (3) ◽  
pp. 320-327 ◽  
Author(s):  
Laura E. White ◽  
Yan Cui ◽  
Carolyn M. Feltes Shelak ◽  
Mihaela L. Lie ◽  
Heitham T. Hassoun
Keyword(s):  
Acute Kidney Injury ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Kidney Injury ◽  
Endothelial Cell Apoptosis ◽  
Ischemic Acute Kidney Injury

scholarly journals PS184. Lung Endothelial Cell Apoptosis during Ischemic Acute Kidney Injury

2012 ◽  
Vol 55 (6) ◽  
pp. 73S-74S
Author(s):  
Laura E. White ◽  
Yan Cui ◽  
Carolyn M. Feltes Shelak ◽  
Heitham T. Hassoun
Keyword(s):  
Acute Kidney Injury ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Kidney Injury ◽  
Endothelial Cell Apoptosis ◽  
Ischemic Acute Kidney Injury

scholarly journals Human heat shock protein 27-overexpressing mice are protected against acute kidney injury after hepatic ischemia and reperfusion

2009 ◽  
Vol 297 (4) ◽  
pp. F885-F894 ◽  
Author(s):  
Sang Won Park ◽  
Sean W. C. Chen ◽  
Mihwa Kim ◽  
Vivette D. D'Agati ◽  
H. Thomas Lee
Keyword(s):  
Acute Kidney Injury ◽  
Endothelial Cell ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Cell Apoptosis ◽  
Kidney Injury ◽  
Heat Shock Protein 27 ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Endothelial Cell Apoptosis ◽  
Liver And Kidney

Liver ischemia-reperfusion injury (IRI) causes acute kidney injury (AKI) in mice characterized by renal endothelial cell apoptosis, renal tubular necrosis, inflammation, and filamentous (F)-actin disruption. Since heat shock protein 27 (HSP27) protects against apoptosis, necrosis, and stabilizes F-actin, we questioned whether overexpression of human HSP27 (huHSP27 OE) in mice would attenuate AKI after liver IRI. Twenty-four hours after hepatic IRI, HSP27 wild-type (WT) mice developed acute liver and kidney injury with elevated plasma alanine aminotransferase and creatinine, a reduced glomerular filtration rate, and histological evidence of renal endothelial cell apoptosis and tubular injury (necrosis, vacuolization, and F-actin disruption). The huHSP27 OE mice, however, were significantly protected against both liver and kidney injury after hepatic IRI. The huHSP27 OE mice also showed less induction of several proinflammatory mRNAs (TNF-α, MIP-2, and keratinocyte-derived cytokine), neutrophil infiltration, and reduction in apoptosis (terminal deoxynucleotidyl transferase biotin-dUTP nick end-labeling assay and DNA laddering) in the kidney compared with the HSP27 WT mice. Moreover, the huHSP27 OE mice showed significantly less disruption of F-actin in renal proximal tubules and better preserved vascular endothelial cell integrity compared with the huHSP27 OE mice. Finally, the kidney plays a major role in the hepatoprotective effects of huHSP27 overexpression as the hepatoprotection was reduced or abolished in mice subjected to unilateral or bilateral nephrectomy, respectively. Our results show that overexpression of huHSP27 protects against hepatic injury and AKI associated with liver IRI in vivo. Harnessing the mechanisms of cytoprotection with renal HSP27 may lead to new therapies for the perioperative AKI and liver injury associated with liver IRI.

Nf-κB Promotes Pulmonary Endothelial Cell Survival During Ischemic Acute Kidney Injury

2012 ◽  
Vol 172 (2) ◽  
pp. 265
Author(s):  
L.E. White ◽  
Y. Cui ◽  
C. M. Feltes Shelak ◽  
F.A. Moore ◽  
H.T. Hassoun
Keyword(s):  
Acute Kidney Injury ◽  
Endothelial Cell ◽  
Cell Survival ◽  
Kidney Injury ◽  
Endothelial Cell Survival ◽  
Ischemic Acute Kidney Injury

Kidney-Lung Crosstalk: Identifying Pulmonary Endothelial Cell-Specific Changes During Ischemic Acute Kidney Injury

2012 ◽  
Vol 172 (2) ◽  
pp. 271
Author(s):  
Y. Cui ◽  
L.E. White ◽  
C.M. Feltes-Shelak ◽  
F.A. Moore ◽  
H.T. Hassoun
Keyword(s):  
Acute Kidney Injury ◽  
Endothelial Cell ◽  
Kidney Injury ◽  
Ischemic Acute Kidney Injury
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